APOL1 Kidney Disease: The Gene Variants Behind Higher Kidney Risk

Table of Contents

1. The APOL1 Gene and the G1 and G2 Variants
2. Why the Variants Are Common: African Sleeping Sickness
3. How Common Two Variants Are
4. Lifetime Risk, Stated Both Ways
5. Kidney Diseases Linked to Two Variants
6. The Second Hit Idea and the Evidence Behind It
7. Kidney Donation and Transplant Findings
8. Genetic Testing as the Sources Describe It
9. Treatments Under Study
10. What Is Not Known
11. Key Research Papers
12. Connections
13. Featured Videos

The APOL1 Gene and the G1 and G2 Variants

The APOL1 gene sits on chromosome 22. It makes a protein that circulates in the blood as part of the body's defence against trypanosomes, the single-celled parasites that cause African sleeping sickness. The protein lyses (breaks open) these parasites.

In 2010 a team led from Boston reported that two variants of this gene, now called G1 and G2, were strongly tied to kidney disease in African Americans. People carrying two copies had odds of focal segmental glomerulosclerosis 10.5 times higher (95% confidence interval 6.0 to 18.4) and odds of kidney failure attributed to high blood pressure 7.3 times higher (5.6 to 9.5) than people without them. The same paper found that both variants were common on African chromosomes and absent from European ones, and that both sat inside stretches of DNA carrying the signature of positive natural selection.

Everyone has two copies of the gene, one from each parent. A person can carry zero, one or two risk variants. The combinations G1/G1, G2/G2 and G1/G2 all count as two variants, the group researchers call the high-risk genotype. Researchers describe the effect as mostly recessive: in the large American studies, the extra risk sits almost entirely with people who have two variants, not one. The 2022 review in Nature Reviews Nephrology states that risk of APOL1 nephropathy "is mostly confined to individuals with two APOL1 risk variants".

The variants are thought to act as a gain of function: the altered protein does something harmful rather than simply failing to work. A 2025 review notes that the gene does not appear to be needed for normal kidney function. Cell studies point to several possible harms, including disturbed ion channels, inflammasome activation, stress in the cell's protein-folding machinery and damage to mitochondria. Those are cell-culture findings; which of them matters most in a human kidney is still debated.

In 2024 an international conference held by Kidney Disease: Improving Global Outcomes (KDIGO) in Accra, Ghana, agreed on a name: APOL1 kidney disease, used alone or with the specific diagnosis added (for example, "APOL1 kidney disease, focal segmental glomerulosclerosis").

Why the Variants Are Common: African Sleeping Sickness

A variant that damages kidneys would normally become rare over many generations. The leading explanation for why G1 and G2 stayed common is that they protected their carriers against a deadly infection. The ordinary APOL1 protein kills most African trypanosomes but not Trypanosoma brucei rhodesiense or Trypanosoma brucei gambiense, the two subspecies that cause human sleeping sickness. In the 2010 laboratory tests, only the kidney-disease variants of the protein killed T. b. rhodesiense. The authors wrote that they "speculate" that this survival advantage may have contributed to the high rates of kidney disease in African Americans.

A 2017 case-control study in Africa tested that idea in people. It found a five-fold protective effect of G2 against T. b. rhodesiense infection, needing only one copy. The results for the other subspecies were not simple: G2 was tied to faster progression of T. b. gambiense sleeping sickness, while G1 was tied to carrying the parasite without symptoms and without detectable parasites in the blood. The authors concluded that both forms of the disease may have shaped how common the variants became.

A 2019 study from Kinshasa in the Democratic Republic of the Congo found G1 in 19.1% and G2 in 7.1% of gene copies tested. No one in the study carried G2/G2. The authors suggested this may reflect strong selection by T. b. gambiense in Central Africa, and that the presence of G2/G2 among people of African ancestry in the United States may reflect the absence of that pressure.

The variants follow ancestry, not the social category of race. A 2011 survey of world populations found the kidney-risk variants only on African chromosomes. Whether a person inherited two variants is shown only by a genetic test. The parasite itself is covered on the Trypanosoma page.

How Common Two Variants Are

Several sources put the share of African Americans with two variants at about 13%. In the Jackson Heart Study in Mississippi, 41.3% of 2,300 genotyped participants had zero variants, 45.1% had one and 13.6% had two. In the long-running Atherosclerosis Risk in Communities study, 3.2% of all 15,140 participants were Black with the high-risk genotype, against 21.5% who were Black without it. A 2025 review estimates that about 6 million African Americans carry two variants.

In West Africa the figures are higher. A 2025 study of 8,355 people in Ghana and Nigeria, which mixed people with and without kidney disease, found one variant in 43.0% and two variants in 29.7%. Because that sample deliberately included many people with kidney disease, it is not a population estimate, but it shows how widespread the variants are in the region.

Most people with recent African ancestry carry zero or one variant. In the American cohorts, one variant was not tied to higher kidney risk: in the Jackson Heart Study, having one variant "was not associated with increased risk for CKD outcomes". The West African study found a small effect of one variant there (odds of chronic kidney disease 18% higher, odds of focal segmental glomerulosclerosis 61% higher), so whether a single copy matters may differ between populations.

Lifetime Risk, Stated Both Ways

The variants raise risk; they do not make kidney failure certain. These are the figures the sources give:

• Kidney failure overall. A 2024 study states that among people with the high-risk genotype, the lifetime risk of kidney failure is about 15%. Put the other way, roughly 85 in 100 people with two variants do not reach kidney failure in their lifetime.
• Focal segmental glomerulosclerosis. The 2011 study estimated a 4% lifetime risk for people with two variants, so about 96 in 100 never develop it.
• Human immunodeficiency virus-associated nephropathy. The same study estimated that people with two variants and untreated human immunodeficiency virus infection have a 50% risk of human immunodeficiency virus-associated nephropathy.
• Chronic kidney disease in the general population. In 3,067 African Americans without kidney disease at the start of the Atherosclerosis Risk in Communities study, two variants were tied to a 1.49-fold higher risk of developing chronic kidney disease and a 1.88-fold higher risk of kidney failure, compared with zero or one.
• In the Jackson Heart Study, two variants were tied to a higher risk of new albumin in the urine (adjusted hazard ratio 1.88), new chronic kidney disease (1.65) and kidney failure (9.05, with a very wide 95% confidence interval of 1.79 to 45.85, reflecting few events).

The same research also shows how much individuals vary. In the Atherosclerosis Risk in Communities study, the yearly fall in estimated glomerular filtration rate overlapped heavily between groups: a median of 1.5 for white participants, 2.1 for Black participants with zero or one variant and 2.3 for Black participants with two variants (all in ml/min per 1.73 m² per year). The authors wrote that this high variability suggests "population-based screening is not yet justified".

Kidney Diseases Linked to Two Variants

The variants are tied to a family of kidney diseases rather than a single one. The strength of the link differs by disease and by study design. Case-control studies (people with the disease compared with people without it) give the largest numbers; community studies that follow healthy people forward give smaller ones.

Focal segmental glomerulosclerosis. In the 2011 study, disease in people with two variants began earlier and progressed to kidney failure faster, but responded to steroids about as often as in other patients. The authors calculated that two variants explain 18% of focal segmental glomerulosclerosis and 35% of human immunodeficiency virus-associated nephropathy in their sample, and that removing the effect would reduce both diseases by 67%.

Kidney disease attributed to high blood pressure. In the African American Study of Kidney Disease and Hypertension trial, kidney failure or a doubling of the blood creatinine level occurred in 58.1% of patients with two variants and 36.6% of those with zero or one (hazard ratio 1.88). The variants' effect did not change with the trial's drug or blood-pressure-target groups. In the companion Chronic Renal Insufficiency Cohort, Black patients with two variants lost kidney function faster than white patients, with or without diabetes. A 2022 review describes this clinical picture as "hypertension and arterionephrosclerosis". The long-running question of whether blood pressure causes this kidney damage or results from it is discussed on the Hypertensive Nephropathy page.

Lupus nephritis. The 2014 study compared 855 African American lupus patients with kidney failure and 534 without kidney disease. Ninety percent were women. Kidney failure arrived about 2 years sooner after the lupus diagnosis in people with two variants. More on the disease itself is on the Lupus Nephritis page.

COVID-19-associated collapsing glomerulopathy. During the pandemic, doctors reported a severe pattern of kidney injury, called collapsing glomerulopathy, in Black patients with COVID-19, closely resembling human immunodeficiency virus-associated nephropathy. In the first series of 6 patients, all had two variants; 5 needed dialysis, 2 of whom died. In a Columbia University series of 23 patients, most had mild or moderate COVID-19, 61% needed dialysis when they arrived and 16 of the 17 genotyped carried two variants. After a median of 155 days, 68% were off dialysis, including 7 of the 14 who had needed it at the start, while 32% had reached kidney failure or death. Neither series found the virus inside kidney cells, which points to the body's inflammatory response rather than direct infection.

Kidney disease in general. A 2023 study of 239 patients with chronic kidney disease and two variants, matched with 1,187 patients of similar genetic ancestry and zero or one variant, found a higher risk of kidney failure (hazard ratio 1.58), a faster yearly fall in estimated glomerular filtration rate (6.55 against 3.63 ml/min/1.73 m²) and kidney failure at a younger age (45.1 against 53.6 years). The G1/G1 combination carried the highest risk. A 2026 review rates the link as robust for focal segmental glomerulosclerosis, human immunodeficiency virus-associated nephropathy and kidney failure attributed to high blood pressure, and inconsistent for diabetic kidney disease.

The Second Hit Idea and the Evidence Behind It

If 85 in 100 people with two variants never reach kidney failure, something else must decide who does. Researchers call this the second hit: the genotype is the first hit, and a later trigger, often an infection or inflammation, is the second. The idea rests on several kinds of evidence of different strength.

• Human cohort data (strongest). Untreated human immunodeficiency virus infection carries a 50% risk of human immunodeficiency virus-associated nephropathy in people with two variants, according to the 2011 estimate. A 2022 review calls chronic viral infection, especially human immunodeficiency virus type 1, "the best recognized" second hit, acting through interferon switching on the APOL1 gene. The same review adds that "most individuals with APOL1 nephropathy do not have an obvious cofactor".
• Case series (weaker, no comparison group). The COVID-19 reports above found collapsing glomerulopathy clustered in patients with two variants and proposed a "two-hit" combination of genetic risk and the body's inflammatory reaction to the virus.
• Animal studies. In mice built to carry the human APOL1 gene under its own human control switch, the animals showed no kidney disease on their own. A dose of the immune signal interferon-gamma caused heavy protein loss in the urine only in mice carrying G1, even though it raised APOL1 levels in both normal and G1 mice.
• Cell studies. Cell-culture work shows the variant proteins harming kidney cells by several routes, but much of it uses cells forced to make large amounts of the protein, a limitation the 2026 review points out.
• Modifier genes (early evidence). The 2023 study found rare variants in inflammasome genes more often in patients with two APOL1 variants and kidney disease (odds ratio 1.90), suggesting other genes may also shape who becomes ill.

One case report complicates the picture. A patient with two variants developed COVID-19-associated collapsing glomerulopathy in a transplanted kidney that came from a donor with a low-risk genotype. The authors wrote that this "contradicts current models" and suggests that APOL1 made inside the kidney "may not be the driver" of the injury.

Kidney Donation and Transplant Findings

The APOL1 genotype that matters in a transplant is mainly the donor kidney's, because the kidney carries the donor's genes.

Kidneys from deceased donors. A 2011 single-centre study followed 136 kidneys from 106 African American deceased donors. Kidneys from donors with two variants failed sooner (hazard ratio 3.84). A 2015 follow-up across 675 transplanted kidneys, with outcomes from 55 United States centres, confirmed the link (hazard ratio 2.26), while African American recipient background was separately tied to graft failure (hazard ratio 1.60). The authors proposed rapid genotyping of African American deceased donors at the time of organ recovery and using the results in allocation and consent.

Living kidney donors. A 2018 study followed 136 Black living donors, 19 of whom (14%) had two variants. At a median of 12 years after donation, those with two variants had lower kidney function (estimated glomerular filtration rate 57 against 67 ml/min per 1.73 m²) and faster decline. Two donors developed kidney failure, and both carried two variants. When donors were compared with non-donors of the same genotype, the rate of decline did not differ, and the authors called for a larger study.

That larger study was published in 2026. It enrolled 445 Black and 208 White people who had donated a kidney in the United States between 2000 and 2008, and visited them at home a median of 18.5 years later. Sixty-eight of the Black donors (15.3%) had two variants. Black donors with two variants were more likely to have an estimated glomerular filtration rate below 45 (relative risk 2.31, 95% confidence interval 1.16 to 4.61). After accounting for kidney function before donation, the relative risk was 1.91, and that result was not statistically significant (95% confidence interval 0.90 to 4.03). The authors concluded that the genotype is a risk factor for reduced kidney function after donation and wrote that their results suggest all Black living-donor candidates in the United States undergo APOL1 genotyping.

A 2019 ethics paper sets out the questions transplant programmes face: when and to whom to offer testing, what potential donors are told, how results affect who may donate, and whether recipients see the results. More on transplant itself is on the Dialysis and Kidney Transplant page.

Genetic Testing as the Sources Describe It

APOL1 testing is a genetic test that reads which versions of the gene a person carries. The sources differ on how useful it is outside specific situations.

• The 2025 conference report states that because there are no established treatments for APOL1 kidney disease and a genotype result is "not by themselves actionable", there is insufficient evidence for population screening or routine testing. It also states that genotyping can help inform risk assessment, how often a person is followed up, living kidney donation and eligibility for clinical trials.
• A 2017 review raised concerns that testing could cause confusion, anxiety or stigma, and called for informed consent and counselling, with the views of community members included.
• The 2016 general-population study concluded that population screening was "not yet justified" because of the large overlap between groups.
• A 2024 study of 15,181 people who had genetic testing for inherited kidney disease found that about 10% of those with two APOL1 variants also had a separate single-gene kidney disease. A high-risk APOL1 result therefore does not rule out another genetic cause. A 2023 study found the same pattern (2.5% against 6.7% in people with fewer than two variants).

Kidney function itself is measured with the estimated glomerular filtration rate, explained on the eGFR and Your CKD Stage page, along with the 2021 change to an equation that no longer uses race.

Treatments Under Study

The 2022 review states that current therapies are not adequate to halt the progression of APOL1 kidney disease. A 2026 review states that management is mainly through medicines that block the renin-angiotensin system, and the 2013 trial data above showed that the genotype's effect persisted whatever blood-pressure treatment was given. Several targeted approaches are in development.

Inaxaplin. Inaxaplin is a small-molecule drug that blocks the channel the APOL1 protein forms. In cells and in a mouse model it reduced APOL1 activity and protein loss in the urine. In a single-group, open-label phase 2a study, 16 people with two variants, biopsy-confirmed focal segmental glomerulosclerosis and protein in the urine took it daily for 13 weeks (15 mg for 2 weeks, then 45 mg for 11 weeks) alongside standard care. In the 13 who took at least 80% of their doses, the urine protein-to-creatinine ratio fell by an average of 47.6% (95% confidence interval 31.3% to 60.0%). Similar reductions were seen in all but 1 participant when everyone was counted. Side effects were mild or moderate and none led anyone to leave the study. The study had no comparison group, and its 13 weeks measured urine protein, not kidney failure.

Two earlier phase 1 studies gave inaxaplin or placebo to 178 healthy volunteers (94.9% male). Side effects of any kind occurred in 24.6% on inaxaplin and 22.7% on placebo; headache was the most common (10.4% against 2.3%). There were no serious side effects and no one stopped because of the drug.

A phase 2/3 trial named AMPLITUDE is now testing inaxaplin against placebo in adults and children with APOL1 kidney disease. Its registration (NCT05312879) describes it as randomized and double-blind, with 522 people enrolled. Its main measures are the change in urine protein at 48 weeks at an interim analysis and the slope of kidney function over at least 2 years. As of the registry's October 2026 update, the trial was active but no longer recruiting, with results not yet posted. A 2025 review describes inaxaplin as "advanced to a phase 3 study". A 2026 review states that, to date, no APOL1-targeted drug has shown benefit on a hard kidney outcome such as kidney failure.

Lowering the amount of APOL1. In the mouse study described above, an antisense drug that blocks the APOL1 message (messenger RNA) lowered APOL1 in the kidney and liver and protected G1 mice from interferon-triggered protein loss, in a dose-dependent way. That was in mice only.

What Is Not Known

• Who among carriers becomes ill. Most people with two variants keep normal kidneys, and in most patients with APOL1 kidney disease no obvious second hit is found.
• How exactly the protein damages the kidney. Several mechanisms are proposed from cell studies, and they are still contested.
• Whether one variant matters. American cohorts found no clear effect of a single copy; the 2025 West African study found a modest one.
• The kidney or the blood. The transplant data point to the kidney's own genotype, while the COVID-19 transplant case suggests APOL1 made inside the kidney may not be the driver.
• Whether treatment changes hard outcomes. Inaxaplin's published result is a 13-week change in urine protein in 16 people without a placebo group; whether it slows kidney failure awaits the phase 2/3 trial.
• Whether testing healthy people helps them. The 2025 conference found the evidence insufficient for population screening.
• The long-term safety of donation for living donors with two variants, beyond about 18 years of follow-up.

The 2013 study concluded that the variants were associated with the higher rates of kidney failure and faster kidney disease progression seen in Black patients compared with white patients, with or without diabetes. The 2016 study adds a second finding: in its fully adjusted analysis the high-risk genotype was tied only to kidney failure, while Black participants as a group still had higher risk of high blood pressure, diabetes and kidney failure after adjustment for other illnesses and for income and education.

Key Research Papers

1. Genovese G, Friedman DJ, Ross MD, Lecordier L, Uzureau P, Freedman BI, et al. Association of trypanolytic ApoL1 variants with kidney disease in African Americans. Science. 2010;329(5993):841-5. PubMed PMID: 20647424
2. Kopp JB, Nelson GW, Sampath K, Johnson RC, Genovese G, An P, et al. APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy. Journal of the American Society of Nephrology. 2011;22(11):2129-37. PubMed PMID: 21997394
3. Cooper A, Ilboudo H, Alibu VP, Ravel S, Enyaru J, Weir W, et al. APOL1 renal risk variants have contrasting resistance and susceptibility associations with African trypanosomiasis. eLife. 2017;6:e25461. PubMed PMID: 28537557
4. Sumaili EK, Shemer R, Kruzel-Davila E, Cohen EP, Mutantu PN, Bukabau JB, et al. G1 is the major APOL1 risk allele for hypertension-attributed nephropathy in Central Africa. Clinical Kidney Journal. 2019;12(2):188-195. PubMed PMID: 30976395
5. Parsa A, Kao WH, Xie D, Astor BC, Li M, Hsu CY, et al. APOL1 risk variants, race, and progression of chronic kidney disease. New England Journal of Medicine. 2013;369(23):2183-96. PubMed PMID: 24206458
6. Foster MC, Coresh J, Fornage M, Astor BC, Grams M, Franceschini N, et al. APOL1 variants associate with increased risk of CKD among African Americans. Journal of the American Society of Nephrology. 2013;24(9):1484-91. PubMed PMID: 23766536
7. Grams ME, Rebholz CM, Chen Y, Rawlings AM, Estrella MM, Selvin E, et al. Race, APOL1 Risk, and eGFR Decline in the General Population. Journal of the American Society of Nephrology. 2016;27(9):2842-50. PubMed PMID: 26966015
8. Young BA, Wilson JG, Reiner A, Kestenbaum B, Franceschini N, Bansal N, et al. APOL1, Sickle Cell Trait, and CKD in the Jackson Heart Study. Kidney Medicine. 2021;3(6):962-973.e1. PubMed PMID: 34939005
9. Gbadegesin RA, Ulasi I, Ajayi S, Raji Y, Olanrewaju T, Osafo C, et al. APOL1 Bi- and Monoallelic Variants and Chronic Kidney Disease in West Africans. New England Journal of Medicine. 2025;392(3):228-238. PubMed PMID: 39465900
10. Elliott MD, Marasa M, Cocchi E, Vena N, Zhang JY, Khan A, et al. Clinical and Genetic Characteristics of CKD Patients with High-Risk APOL1 Genotypes. Journal of the American Society of Nephrology. 2023;34(5):909-919. PubMed PMID: 36758113
11. da Silva Francisco R Jr, Punj S, Vincent L, Sanapareddy N, Bhalla V, Chertow GM, et al. Prevalence of Mendelian Kidney Disease Among Patients With High-Risk APOL1 Genotypes Undergoing Commercial Genetic Testing in the United States. Kidney International Reports. 2024;9(9):2667-2676. PubMed PMID: 39291188
12. Freedman BI, Langefeld CD, Andringa KK, Croker JA, Williams AH, Garner NE, et al. End-stage renal disease in African Americans with lupus nephritis is associated with APOL1. Arthritis & Rheumatology. 2014;66(2):390-6. PubMed PMID: 24504811
13. Wu H, Larsen CP, Hernandez-Arroyo CF, Mohamed MMB, Caza T, Sharshir M, et al. AKI and Collapsing Glomerulopathy Associated with COVID-19 and APOL 1 High-Risk Genotype. Journal of the American Society of Nephrology. 2020;31(8):1688-1695. PubMed PMID: 32561682
14. Kudose S, Santoriello D, Bomback AS, Sekulic M, Batal I, Stokes MB, et al. Longitudinal Outcomes of COVID-19-Associated Collapsing Glomerulopathy and Other Podocytopathies. Journal of the American Society of Nephrology. 2021;32(11):2958-2969. PubMed PMID: 34670811
15. Shetty AA, Tawhari I, Safar-Boueri L, Seif N, Alahmadi A, Gargiulo R, et al. COVID-19-Associated Glomerular Disease. Journal of the American Society of Nephrology. 2021;32(1):33-40. PubMed PMID: 33214201
16. Daneshpajouhnejad P, Kopp JB, Winkler CA, Rosenberg AZ. The evolving story of apolipoprotein L1 nephropathy: the end of the beginning. Nature Reviews Nephrology. 2022;18(5):307-320. PubMed PMID: 35217848
17. Aghajan M, Booten SL, Althage M, Hart CE, Ericsson A, Maxvall I, et al. Antisense oligonucleotide treatment ameliorates IFN-γ-induced proteinuria in APOL1-transgenic mice. JCI Insight. 2019;4(12):e126124. PubMed PMID: 31217349
18. Reeves-Daniel AM, DePalma JA, Bleyer AJ, Rocco MV, Murea M, Adams PL, et al. The APOL1 gene and allograft survival after kidney transplantation. American Journal of Transplantation. 2011;11(5):1025-30. PubMed PMID: 21486385
19. Freedman BI, Julian BA, Pastan SO, Israni AK, Schladt D, Gautreaux MD, et al. Apolipoprotein L1 gene variants in deceased organ donors are associated with renal allograft failure. American Journal of Transplantation. 2015;15(6):1615-22. PubMed PMID: 25809272
20. Doshi MD, Ortigosa-Goggins M, Garg AX, Li L, Poggio ED, Winkler CA, et al. APOL1 Genotype and Renal Function of Black Living Donors. Journal of the American Society of Nephrology. 2018;29(4):1309-1316. PubMed PMID: 29339549
21. Hsu CY, Gao Y, Freedman BI, Lunn MR, Muiru AN, Schnitzler MA, et al. Apolipoprotein L1 Gene Genotype and Kidney Outcomes After Living Kidney Donation. JAMA Internal Medicine. 2026;186(8):943-950. PubMed PMID: 42329639
22. Mohan S, Iltis AS, Sawinski D, DuBois JM. APOL1 Genetic Testing in Living Kidney Transplant Donors. American Journal of Kidney Diseases. 2019;74(4):538-543. PubMed PMID: 30982552
23. Young BA, Fullerton SM, Wilson JG, Cavanaugh K, Blacksher E, Spigner C, et al. Clinical Genetic Testing for APOL1: Are we There Yet? Seminars in Nephrology. 2017;37(6):552-557. PubMed PMID: 29110763
24. Ojo AO, Adu D, Bramham K, Freedman BI, Gbadegesin RA, Ilori TO, et al. APOL1 kidney disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney International. 2025;108(5):763-779. PubMed PMID: 40582702
25. Egbuna O, Zimmerman B, Manos G, Fortier A, Chirieac MC, Dakin LA, et al. Inaxaplin for Proteinuric Kidney Disease in Persons with Two APOL1 Variants. New England Journal of Medicine. 2023;388(11):969-979. PubMed PMID: 36920755
26. Egbuna O, Audard V, Manos G, Tian S, Hagos F, Chertow GM. Safety and Tolerability of the APOL1 Inhibitor, Inaxaplin, following Single- and Multiple-Ascending Doses in Healthy Adults. Glomerular Diseases. 2024;4(1):64-73. PubMed PMID: 38600955
27. Srinivasan V, So PN, Kwakyi EPK, Lerma EV, Wiegley N. APOL1 Mediated Kidney Disease: A Review and Look Toward the Future. Kidney Medicine. 2025;7(9):101062. PubMed PMID: 40837248
28. Dogra N, Baranwal M, Ahmad S, Kumar P, Ashawat MS. APOL1 kidney disease: a critical narrative review of molecular mechanisms, clinical heterogeneity, and the emerging therapeutic landscape. International Urology and Nephrology. 2026 (online ahead of print). PubMed PMID: 42709370

PubMed Topic Searches

1. PubMed: APOL1 kidney disease
2. PubMed: APOL1 and trypanosomes
3. PubMed: APOL1, kidney donors and transplant
4. PubMed: APOL1 and COVID-19 collapsing glomerulopathy
5. PubMed: inaxaplin

Connections

• Nephrology & Hepatology — the kidney and liver category
• Focal Segmental Glomerulosclerosis (FSGS) — the disease most tied to two variants
• Hypertensive Nephropathy — kidney disease attributed to high blood pressure
• Chronic Kidney Disease — stages, causes and care
• Nephrotic Syndrome — heavy protein loss in the urine
• Lupus Nephritis — lupus in the kidney
• Dialysis and Kidney Transplant — treatment when kidneys fail
• eGFR and Your CKD Stage — how kidney function is measured
• Trypanosoma — the sleeping-sickness parasite behind the variants

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